Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urinary tract infections, most of which are biofilm infections in catheterized patients, account for more than 40% of hospital infections. Bacterial colonization of the urinary tract and catheters causes not only infection but also other complications such as catheter blockage by bacterial encrustation, urolithiasis and pyelonephritis. About 50% of long-term catheterized patients face urinary flow obstruction due to catheter encrustation, but no measure is currently available to prevent it. Encrustation has been known either to result from metabolic dysfunction or to be of microbial origin, with urease positive bacterial species implicated most often. Infectious calculi account for about 15-20% of all cases of urolithiasis and are often associated with biofilm colonization of a long-term indwelling urinary catheter or urethral stent. The use of closed catheter systems is helpful in reducing such problems; nevertheless, such a system only delays the inevitable, with infections emerging a little later. Various coatings intended to prevent the bacterial adhesion to the surface of catheters and implants and thus also the emergence of biofilm infections, unfortunately, do not inhibit the microbial adhesion completely and permanently and the only reliable method for biofilm eradication remains the removal of the foreign body from the patient.
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PMID:[Urinary catheter biofilm infections]. 1857 9

The Gram-negative bacterium Proteus mirabilis causes urinary tract infections (UTIs) in individuals with long-term indwelling catheters or those with functional or structural abnormalities of the urinary tract. Known virulence factors include urease, haemolysin, fimbriae, flagella, DsbA, a phosphate transporter and genes involved in cell-wall synthesis and metabolism, many of which have been identified using the technique of signature-tagged mutagenesis (STM). To identify additional virulence determinants and to increase the theoretical coverage of the genome, this study generated and assessed 1880 P. mirabilis strain HI4320 mutants using this method. Mutants with disruptions in genes vital for colonization of the CBA mouse model of ascending UTI were identified after performing primary and secondary in vivo screens in approximately 315 CBA mice, primary and secondary in vitro screens in both Luria broth and minimal A medium to eliminate mutants with minor growth deficiencies, and co-challenge competition experiments in approximately 500 CBA mice. After completion of in vivo screening, a total of 217 transposon mutants were attenuated in the CBA mouse model of ascending UTI. Following in vitro screening, this number was reduced to 196 transposon mutants with a probable role in virulence. Co-challenge competition experiments confirmed significant attenuation for 37 of the 93 transposon mutants tested, being outcompeted by wild-type HI4320. Following sequence analysis of the 37 mutants, transposon insertions were identified in genes including the peptidyl-prolyl isomerases surA and ppiA, glycosyltransferase cpsF, biopolymer transport protein exbD, transcriptional regulator nhaR, one putative fimbrial protein, flagellar M-ring protein fliF and hook protein flgE, and multiple metabolic genes.
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PMID:Identification of virulence determinants in uropathogenic Proteus mirabilis using signature-tagged mutagenesis. 1871 75

Bacteria have a basic survival strategy: to colonize surfaces and grow as biofilm communities embedded in a gel-like polysaccharide matrix. The catheterized urinary tract provides ideal conditions for the development of enormous biofilm populations. Many bacterial species colonize indwelling catheters as biofilms, inducing complications in patients' care. The most troublesome complications are the crystalline biofilms that can occlude the catheter lumen and trigger episodes of pyelonephritis and septicemia. The crystalline biofilms result from infection by urease-producing bacteria, particularly Proteus mirabilis. Urease raises the urinary pH and drives the formation of calcium phosphate and magnesium phosphate crystals in the biofilm. All types of catheter are vulnerable to encrustation by these biofilms, and clinical prevention strategies are clearly needed, as bacteria growing in the biofilm mode are resistant to antibiotics. Evidence indicates that treatment of symptomatic, catheter-associated urinary tract infection is more effective if biofilm-laden catheters are changed before antibiotic treatment is initiated. Infection with P. mirabilis exposes the many faults of currently available catheters, and plenty of scope exists for improvement in both their design and production; manufacturers should take up the challenge to improve patient outcomes.
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PMID:Bacterial biofilms in patients with indwelling urinary catheters. 1885 7

Rheumatoid arthritis is a crippling and disabling joint disease affecting over 20 million people. It occurs predominantly in women and smokers, and affects the HLA-DR1/4 individuals who carry the "shared epitope" of amino acids EQRRAA. The cause of this disease was investigated by the methods of the philosopher of science Karl Popper who suggested that scientific research should be based on bold conjectures and critical refutations. The "Popper sequences" generate new facts which then change or alter the original problem. The new facts must then be explained by any new theory. Using the "molecular mimicry" model, it was found that Proteus bacteria possess an amino acid sequence ESRRAL in haemolysin which resembles the, shared epitope, and another sequence in urease which resembles type XI collagen. Antibodies to Proteus bacteria have been found in 14 different countries. It would appear that rheumatoid arthritis is caused by an upper urinary tract infection by Proteus bacteria. Anti-Proteus therapy should be assessed in the management of this disease separately or in conjunction with existing modalities of therapy.
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PMID:Rheumatoid arthritis is caused by Proteus: the molecular mimicry theory and Karl Popper. 1948 74

Urologic complications are an important cause of morbidity and even mortality in patients with spinal cord injury (SCI). It has been estimated that within eight years after injury, approximately 7% of SCI patients would develop kidney stones, whereas 36% would have bladder stones. Risk factors for urolithiasis among patients with SCI include complete spinal cord injury, lesions at or above the 4th thoracic spinal cord segment, upper motor neurone type of bladder, urinary tract infection with urease producing bacteria, recurrent urinary tract infection, indwelling catheters, presence of residual urine and immobilization. Detection and removal of bladder stones are important to prevent possible complications such as recurrent urinary tract infection, urosepsis and renal failure. The authors describe a clinical case of a patient with acute SCI that developed bladder stones and discuss its possible causes.
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PMID:[Bladder stones in acute spinal cord injury]. 2035 15

The urinary tract is a common site of bacterial infections; nearly half of all women experience at least one urinary tract infection (UTI) during their lifetime. These infections are classified based on the condition of the host. Uncomplicated infections affect otherwise healthy individuals and are most commonly caused by uropathogenic Escherichia coli, whereas complicated infections affect patients with underlying difficulties, such as a urinary tract abnormality or catheterization, and are commonly caused by species such as Proteus mirabilis. Virulence and fitness factors produced by both pathogens include fimbriae, toxins, flagella, iron acquisition systems, and proteins that function in immune evasion. Additional factors that contribute to infection include the formation of intracellular bacterial communities by E. coli and the production of urease by P. mirabilis, which can result in urinary stone formation. Innate immune responses are induced or mediated by pattern recognition receptors, antimicrobial peptides, and neutrophils. The adaptive immune response to UTI is less well understood. Host factors TLR4 and CXCR1 are implicated in disease outcome and susceptibility, respectively. Low levels of TLR4 are associated with asymptomatic bacteriuria while low levels of CXCR1 are associated with increased incidence of acute pyelonephritis. Current research is focused on the identification of additional virulence factors and therapeutic or prophylactic targets that might be used in the generation of vaccines against both uropathogens.
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PMID:Host-pathogen interactions in urinary tract infection. 2064 92

The oligopeptide transport systems Opp belong to the nickel/peptide/opine PepT subfamily of ABC-transporters. The opportunist pathogen Staphylococcus aureus encodes four putative Opps and one orphean substrate binding protein Opp5A. Here, we report that the Opp2 permease complex (Opp2BCDF) and Opp5A are involved in nickel uptake and then renamed them NikBCDE and NikA respectively. S. aureus carries also a high-affinity nickel transporter NixA belonging to the NiCoT family of secondary transporters. The activity of these two nickel transporters determine that of urease, a multimeric nickel-dependent enzyme mainly involved in the neutralization of acidic environments. However, only the Nik system was responsible for the neutralization and deposit of pH-dependent crystals in human urine. Inactivation of the nik genes affected bacterial colonization of mouse urinary tract, as well as the 50% infective dose levels compared with the parental and nixA strains. Finally, complementation of the nik mutations restored bacterial colonization. Together, our results suggest a role for the Nik system in the urinary tract infection by S. aureus, probably due to the urease-mediated pH increase of the urine.
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PMID:A nickel ABC-transporter of Staphylococcus aureus is involved in urinary tract infection. 2066 75

Nephrolithiasis is a common clinical entity, and the incidence of renal stones appears to be increasing in the United States. Infection with uropathogens that produce urease can lead to the development of stones (infection stones), which serve as a continued source of recurrent infection and can lead to chronic kidney disease. Other than treating infection, medical management has little role in the treatment of infection stones; complete eradication of the stones with percutaneous nephrolithotomy or extracorporeal shock wave lithotripsy is required. Stones of metabolic origin can cause obstruction in the ureter and predispose to the development of urinary tract infection (UTI). Recognizing obstruction and initiating prompt drainage of the collecting system is important in the successful management of nephrolithiasis complicated by UTI. These patients are often at high risk of infection with an antimicrobial-resistant pathogen, so careful consideration of antimicrobial therapy is required, especially for patients who present with severe sepsis.
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PMID:Management of urinary tract infections associated with nephrolithiasis. 2130 54

The enteric bacterium Proteus mirabilis is a common cause of complicated urinary tract infections. In this study, microarrays were used to analyze P. mirabilis gene expression in vivo from experimentally infected mice. Urine was collected at 1, 3, and 7 days postinfection, and RNA was isolated from bacteria in the urine for transcriptional analysis. Across nine microarrays, 471 genes were upregulated and 82 were downregulated in vivo compared to in vitro broth culture. Genes upregulated in vivo encoded mannose-resistant Proteus-like (MR/P) fimbriae, urease, iron uptake systems, amino acid and peptide transporters, pyruvate metabolism enzymes, and a portion of the tricarboxylic acid (TCA) cycle enzymes. Flagella were downregulated. Ammonia assimilation gene glnA (glutamine synthetase) was repressed in vivo, while gdhA (glutamate dehydrogenase) was upregulated in vivo. Contrary to our expectations, ammonia availability due to urease activity in P. mirabilis did not drive this gene expression. A gdhA mutant was growth deficient in minimal medium with citrate as the sole carbon source, and loss of gdhA resulted in a significant fitness defect in the mouse model of urinary tract infection. Unlike Escherichia coli, which represses gdhA and upregulates glnA in vivo and cannot utilize citrate, the data suggest that P. mirabilis uses glutamate dehydrogenase to monitor carbon-nitrogen balance, and this ability contributes to the pathogenic potential of P. mirabilis in the urinary tract.
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PMID:Transcriptome of Proteus mirabilis in the murine urinary tract: virulence and nitrogen assimilation gene expression. 2150 83

We investigated the activity of curcumin against Proteus mirabilis and the struvite crystallization in relation to urinary stones formation. In order to evaluate an activity of curcumin we performed an in vitro experiment of struvite growth from artificial urine. The crystallization process was induced by Proteus mirabilis to mimic the real urinary tract infection, which usually leads to urinary stone formation. The results demonstrate that curcumin exhibits the effect against Proteus mirabilis inhibiting the activity of urease-an enzyme produced by these microorganisms. Addition of curcumin increases the induction time and decreases the efficiency of growth of struvite compared with the absence of curcumin. Interestingly, the addition of curcumin does not affect the crystal morphology and habit. In conclusion, curcumin has demonstrated its significant potential to be further investigated for its use in the case of struvite crystallization induced for the growth by Proteus mirabilis in relation to urinary stone formation.
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PMID:Effect of Curcumin Against Proteus mirabilis During Crystallization of Struvite from Artificial Urine. 2180 56


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